Response Letters Regarding Article, “Masking Inferior Infarction by Anterior Myocardial Injury”
We thank the authors of the 4 letters to the editor for their interest in our work.1 All of the letters raise the interesting and important issue of lead misplacement, which is indeed suggested when one compares the morphology of the P waves in the limb leads in Figure 2 against Figure 1 and Figure 3 in our article. However, the authors of the letters might not have considered other elements on the ECG tracings that do not support such an interpretation. In extensive anterior myocardial injury, there is concordant ST elevation in lead I and aVL; only in high lateral MI might the ST elevation be limited to lead I and aVL. The concordance is clearly seen in lead I and aVL in Figure 2. If, on the other hand, the left-arm and left-leg leads are interchanged, as suspected, then the aVF in Figure 2 would be really aVL and should, therefore, show significant ST elevation concordant to anterior myocardial injury; and lead II, which would be lead “I,” should also show significant ST elevation. Furthermore, leads II, III, and aVF (baseline, Figure 1 and 3) have some slight but persistent ST elevation. On development of an anterior myocardial injury (Figure 2), ST in aVF became flat and somewhat depressed, whereas ST in lead II was still slightly elevated, although markedly decreased compared with ST elevation in lead II of Figure 3. This suggests reciprocal changes in inferior leads as well. Devoid of characteristic P-wave changes, repolarization concordance suggests no lead misplacement.
Whether repolarization concordance should prevail over P-wave changes in determining lead misplacement would depend on how absolute the value of P waves is in diagnosing lead misplacement. A very elegant work by Ho and Ho2 has drawn up an algorithm to detect lead misplacement on the basis of the invariability of counterclockwise loops of normal P waves, with clockwise P loops being a hallmark of lead misplacement. However, Ho and Ho2 clearly specify the limitations of the algorithm in the presence of interatrial conduction delay and left atrial enlargement. A maximum P duration of 140 ms is seen in aVR, and there is a “chad”-like notching of P waves in leads I and II (Figure 2), which suggests interatrial conduction delay and left atrial enlargement. The voltage levels of P waves in leads I and II are almost the same, but in the case of left-arm/left-leg interchanges, P in lead II should be markedly decreased. No doubt, there is also terminal peaking of P in lead III, but there also is elevation of the PR segment for almost 50 ms, which can be seen clearly by comparison with simultaneous PR of lead II. This suggests that the terminal peaking of the P wave in lead III (Figure 2) is associated with some repolarization abnormality of the P wave. Finally, one issue has to be emphasized. The value of a clockwise P loop in diagnosing lead misplacement was determined by deliberate misplacement of leads without any dynamic ischemic state (Ho and Ho2); whether ischemia can alter the P loop from counterclockwise to clockwise has to be determined by further studies.
Dr Casella raises the issue of how inferior Q waves can change without the QRS changes in anterior leads, and this is valid. In an article by Bassan et al,3 the crux of the issue was unmasking of old Q waves in inferior leads by relief of anterior ischemia with coronary artery bypass grafting. However, there were R-wave changes in only 2 of 4 cases.